Figure 2.

The concept of “sebaceous immunobiology”. Sebum production and composition is regulated by intrinsic (i.e. activators of PPAR and RXR nuclear receptors such as prostaglandins, linoleic acid and endocannabinoids) and extrinsic (i.e. androgens, IGF1, insulin, leptin and retinoic acid) factors. Although the primary role of the lipid rich sebum is to lubricate the hair and to contribute to the lipid barrier of the skin, the composing lipids may penetrate also into the dermis (marked with red arrows). Therefore, they may modulate the functions of keratinocytes, immune cells and presumably of stromal cells by altering their gene and protein expression. Importantly, sebocytes are also able not only to respond to but also to produce a large number of cytokines and chemokines which may be important in maintaining the physiological dermal immune milieu such as the Th17 signature of the sebaceous gland rich skin or hair growth. Regarding its interactions with the microbiota, sebum lipids exert antimicrobial effects, may modulate the macrophage – P. acnes interaction, but are also converted by various microbes into lipids with inflammatory properties, which could have a role not just in the pathogenesis of acne but also in other diseases. These altogether support that a change in the amount and composition of the sebum could modulate (patho)physiological settings and thus may be therapeutic target as well. DCs, dendritic cells; FFA, free fatty acids; IDF1, insulin-like growth factor 1; PPAR, peroxisome proliferator-activated receptors; RAR, retinoic acid receptors; RXR, retinoid X receptors; SG, sebaceous gland; TSLP, thymic stromal lymphopoietin.